Australian Doctor Australian Doctor 28th July 2017 | Page 22

How to Treat – Paediatric eye – the first 12 months
Birth marks and lid lesions
NUMEROUS lid and facial lesions
with the potential for ocular
sequelae may be present at birth or
develop soon thereafter.
A
B
C
Facial capillary vascular
malformation
When these lesions, also known as
port-wine stains, involve the upper
eyelid, there is a significant risk of
secondary glaucoma. These children
need regular ophthalmic reviews for
the purpose of screening (and where
it exists, treatment) of glaucoma.
Choroidal vascular malformations
are commonly associated, and neu-
rological complications such as epi-
lepsy and developmental delay may
also be associated.
D
E
Figure 7A. Facial capillary vascular malformation.
Figures 7B and 7C. Capillary haemangioma.
Figure 7D. Orbital dermoid cyst.
Figure 7E. Chalazion.
Capillary haemangioma
These lesions, also known as
strawberry naevi, are bright red/
pink and often involve the face and
eyelid. They can continue to grow
during the first two years of life,
then begin to involute. If the eyelid
is involved, it can cause a mechani-
cal ptosis or astigmatism, both of
which can cause amblyopia. Treat-
ment with topical or systemic pro-
pranolol, under the supervision of
a paediatrician, can be considered
in troublesome cases.
Orbital dermoid cyst
These congenital cysts are usually
found at the junction of the mid-
dle and outer thirds of the upper
orbital rim. When the child becomes
mobile, they are at risk of rupture, so
it is appropriate to consider surgical
removal early in the toddler years.
Some cysts have a posterior exten-
sion that may require pre-operative
imaging and the involvement of an
orbital surgeon.
Delayed visual maturation
THIS is a diagnosis of exclusion
and can be only be made retrospec-
tively. The baby’s visual responses
are less than what are expected for
age, but eventually they do catch
up. It can be a fraught experience
for parents and families, who may
require a lot of time and support.
Important clinical features of
the most common form of delayed
visual
maturation
presenting
to general practice include: the
absence of any systemic disease or
seizure disorder; the eye is struc-
turally normal; ocular alignment
is normal; and neuroimaging and
electrophysiological testing of the
visual system is within normal lim-
its.
The condition needs to be dis-
tinguished from cortical visual
impairment, which usually occurs
in the context of severe perinatal
compromise and hypoxia, and is
often accompanied by neurodevel-
opmental delay.
It is appropriate to refer chil-
dren for an ophthalmic assessment
if they are not reaching the stan-
dard visual response milestones,
namely: blinking to bright light
within a few days of birth; fixing
by six weeks; following by three
months; and maintaining good
ocular alignment by four months
of age.
The natural history of delayed
visual maturation is spontaneous
improvement that often occurs
rapidly. Parents have been known
to comment: “It’s like a switch
was flicked and now they can see.”
Only once this has occurred and
the im